Magnolol Protects Osteoblastic MC3T3-E1 Cells Against Antimycin A-Induced Cytotoxicity Through Activation of Mitochondri
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Magnolol Protects Osteoblastic MC3T3-E1 Cells Against Antimycin A-Induced Cytotoxicity Through Activation of Mitochondrial Function Eun Mi Choi1,2
Abstract—Antimycin A treatment of cells blocks the mitochondrial electron transport chain and leads to elevated ROS generation. In the present study, we investigated the protective effects of magnolol, a hydroxylated biphenyl compound isolated from Magnolia officinalis, on antimycin Ainduced toxicity in osteoblastic MC3T3-E1 cells. Osteoblastic MC3T3-E1 cells were pre-incubated with magnolol before treatment with antimycin A. Cell viability and mineralization of osteoblasts were assessed by MTT assay and Alizarin Red staining, respectively. Mitochondrial dysfunction in cells was measured by mitochondrial membrane potential (MMP), complex IV activity, and ATP level. The cellular antioxidant effect of magnolol in osteoblastic MC3T3-E1 cells was assessed by measuring cardiolipin oxidation, mitochondrial superoxide levels, and nitrotyrosine content. Phosphorylated cAMP-response element-binding protein (CREB ) was evaluated using ELISA assay. Pretreatment with magnolol prior to antimycin A exposure significantly reduced antimycin A-induced osteoblast dysfunction by preventing MMP dissipation, ATP loss, and CREB inactivation. Magnolol also reduced cardiolipin peroxidation, mitochondrial superoxide, and nitrotyrosine production induced by antimycin A. These results suggest that magnolol has a protective effect against antimycin A-induced cell damage by its antioxidant effects and the attenuation of mitochondrial dysfunction. All these data indicate that magnolol may reduce or prevent osteoblast degeneration in osteoporosis or other degenerative disorders. KEY WORDS: magnolol; mitochondrial dysfunction; MC3T3-E1 cells; oxidative stress; CREB.
INTRODUCTION Postmenopausal osteoporosis is a disease in which there is net bone loss because of an imbalance between osteoclast-mediated bone resorption and osteoblast-mediated bone formation [1]. The clinical complications include fractures, disability, and chronic pain. It is estimated that 54% of women aged 50 and older will sustain an osteoporotic fracture during their lifetime [2]. Osteoporosis has been a major public health threat for the elderly, particularly for postmenopausal women. 1
Department of Food and Nutrition, Education Graduate School, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul 130-701, South Korea 2 To whom correspondence should be addressed at Department of Food and Nutrition, Education Graduate School, Kyung Hee University, 1, Hoegi-dong, Dongdaemun-gu, Seoul 130-701, South Korea. E-mail: [email protected]
1204 0360-3997/12/0300-1204/0 # 2012 Springer Science+Business Media, LLC
Oxidative stress, resulting from excessive levels of reactive oxygen species (ROS), represents a major cause of cellular damage and death in a plethora of pathological conditions including osteoporosis, in which there are markedly increased blood levels of oxidative stress markers [3]. Osteoblasts can produce antioxidants such
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